Send to

Choose Destination
Am J Physiol Endocrinol Metab. 2016 Nov 1;311(5):E836-E849. doi: 10.1152/ajpendo.00303.2016. Epub 2016 Sep 27.

Protein coingestion with alcohol following strenuous exercise attenuates alcohol-induced intramyocellular apoptosis and inhibition of autophagy.

Author information

Mary MacKillop Institute for Health Research, Centre for Exercise and Nutrition, Australian Catholic University, Melbourne, Victoria, Australia.
Bond Institute of Health and Sport and Faculty of Health Sciences and Medicine, Bond University, Robina, Queensland, Australia; and.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
Mary MacKillop Institute for Health Research, Centre for Exercise and Nutrition, Australian Catholic University, Melbourne, Victoria, Australia;


Alcohol ingestion decreases postexercise rates of muscle protein synthesis, but the mechanism(s) (e.g., increased protein breakdown) underlying this observation is unknown. Autophagy is an intracellular "recycling" system required for homeostatic substrate and organelle turnover; its dysregulation may provoke apoptosis and lead to muscle atrophy. We investigated the acute effects of alcohol ingestion on autophagic cell signaling responses to a bout of concurrent (combined resistance- and endurance-based) exercise. In a randomized crossover design, eight physically active males completed three experimental trials of concurrent exercise with either postexercise ingestion of alcohol and carbohydrate (12 ± 2 standard drinks; ALC-CHO), energy-matched alcohol and protein (ALC-PRO), or protein (PRO) only. Muscle biopsies were taken at rest and 2 and 8 h postexercise. Select autophagy-related gene (Atg) proteins decreased compared with rest with ALC-CHO (P < 0.05) but not ALC-PRO. There were parallel increases (P < 0.05) in p62 and PINK1 commensurate with a reduction in BNIP3 content, indicating a diminished capacity for mitochondria-specific autophagy (mitophagy) when alcohol and carbohydrate were coingested. DNA fragmentation increased in both alcohol conditions (P < 0.05); however, nuclear AIF accumulation preceded this apoptotic response with ALC-CHO only (P < 0.05). In contrast, increases in the nuclear content of p53, TFEB, and PGC-1α in ALC-PRO were accompanied by markers of mitochondrial biogenesis at the transcriptional (Tfam, SCO2, and NRF-1) and translational (COX-IV, ATPAF1, and VDAC1) level (P < 0.05). We conclude that alcohol ingestion following exercise triggers apoptosis, whereas the anabolic properties of protein coingestion may stimulate mitochondrial biogenesis to protect cellular homeostasis.


alcohol; apoptosis; autophagy; exercise; protein

[Indexed for MEDLINE]
Free full text

Publication types, MeSH terms, Substances

Publication types

MeSH terms


Supplemental Content

Full text links

Icon for Atypon
Loading ...
Support Center